CERIC Center of Excellence for Research on Inflammation and Cardiovascular disease

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Professor of Microbial Pathogenesis Department of Medicine Center for Molecular Medicine, L8:03 Karolinska Institutet at Karolinska Hospital

Phone +46 8 517 734 31

Group members

Post-doctoral fellows


Jenny Odeberg, PhD
Piotr Religa. MD,PhD
Afsar Rahbar, PhD
Stefania Varani, MD,PhD

Graduate students


Mohammed Homman
Klas Strååt
Nina Wolmer Solberg
Madeleine Frederich
Monika Grudzinska, MD
Mensur Dzabic
Soley Omarsdottir, MD

Technical personnel


Charlotte Tammik, medical technologist

Graduate students not yet registered


Xingling Xu, MD, PhD student
Frida Herrgård, MD, PhD student
Chato Taher, MD

Independent senior investigator

Rickard Glas, MD, PhD
Hong Qui, PhD
Rainer de Klark MSc
Giulio Preta, PhD

Cecilia Söderberg-Naucler

Recent evidence suggests that a previously unnoticed cytomegalovirus (CMV) infection can be detected in tissue specimens from patients with many inflammatory diseases such as cardiovascular diseases, autoimmune diseases as well as certain cancers. CMV infects and is carried by 70-100% of the world’s population. For many years, CMV was not considered to be a major human pathogen, since the virus only caused rare cases of CMV inclusion disease in neonates. CMV is an important pathogen in immunosuppressed patients such as transplant patients and AIDS patients. CMV disease in these groups of patients has also high-lightened the role of the virus in the development of other inflammatory diseases.

CMV can produce over 250 proteins, of which approximately 50 are essential for virus replication. Thus, the vast majority of the viral proteins are devoted to control important cellular and immunological functions that will assist the virus to co-exist with its host. We can now detect an active CMV infection in the vast majority of patients with different rheumatic diseases. Thus, 200 CMV encoded proteins will be present in tissues and may for example aggravate inflammation and control vascular changes and fibrosis development. In support of this hypothesis, we have demonstrated that a CMV protein, US28 induces smooth muscle cell migration with relevance for vascular diseases development, that CMV induces LTB4 production in smooth muscle cells and that infection controls MMP/TIMP functions in macrophages; both with relevance for inflammation and fibrosis development. This project is focused on understanding how CMV through its unique ability to control host cell functions can contribute to the pathogenesis of inflammatory diseases. Our project includes two separate projects. The long-term goals of these projects are:
  • To further understand how CMV is involved in the development of inflammatory diseases.
  • To further understand the role of CMV as a link between rheumatic diseases and cardiovascular diseases.

Research interactions with CERIC

  • Determine the prevalence of an active CMV infection in patients with different autoimmune diseases and cardiovascular diseases. –Is reactivation of CMV a risk factor for the development of cardiovascular diseases?
  • Further investigate how CMV induces and maintain inflammation; these studies include focus on 5-LO, cox-2, PGES pathways as well as the viral control of immunomodulatory cytokines such as IL-10 and TGF-b.
  • Examine whether CMV affect the production and biological activity of LL37.
  • Further determine the relevance of CD28 negative T cells in autoimmunity, CMV infection and cardiovascular disease.